Chapter 18 Myofascial Pain Flashcards

1
Q

Myofascial pain disorders

A

heterogeneous group of
clinical entities that share features that originate from
soft tissue pain with resultant regional symptomatology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Examples of Myofascial Pain Disorders

A

episodic tension-type headache, myofascial pain syndrome, temporomandibular disorder, muscle cramps, and low back pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Muscle pain is thought to occur by two main mechanisms:

A

peripheral and central

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Peripheral factors of muscle pain

A

trauma, dysregulated deep-tissue microcirculation, and altered muscular metabolism and mitochondrial function. Mechanical, thermal, or chemical stimulation can lead to activation of intramuscular group III and group IV nociceptors, which in turn give rise to an inflammatory cascade mediated by immune cells, leading to further recruitment
of inflammatory cells and propagation of local inflammation and sensitization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Central factors of muscle pain

A

Pain transmission occurs along
Ad and C-fibers into the inner lamina of the spinal cord, where complex changes occur, leading to sensitization and
chronic pain. Continuous nociceptive input via these pathways can lead to central sensitization of higher-order neurons, –> enhanced sensitivity to painful stimuli via
excitatory glutamate and aspartate-related neurotransmitter release (hyperalgesia),reduced thresholds to nonpainful stimuli (allodynia), and increased receptive fields, causing referred pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Supraspinal mechanisms contribute to chronic muscular pain states include

A

decreased cerebral activity, hippocampal suppression, and possibly impaired stress responses. Once central sensitization occurs, pain becomes autonomous from sensory input from the affected
muscle(s)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

The International Headache Society classifies tension-type

headaches (TTHs) as

A

infrequent episodic (,12 days/yr), frequent episodic (12 to fewer than 180 days/yr), and chronic (180 days/yr).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Pathophysiologic mechanisms responsible for TTH can be divided into

A

peripheral and central causes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Peripheral factors of tension-type headaches

A

Peripheral mechanisms are demonstrated by increased tenderness of pericranial myofascial tissue and increased electromyographic
and algometric pressure recordings

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Central factors of tension-type headaches

A

Continuous nociceptive

input can lead to central sensitization, thereby converting episodic TTH into chronic headaches

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Temporomandibular disorder (TMD)

A

is a broad term used to describe conditions arising in the jaw joint, muscles of mastication, and associated craniofacial structures. These conditions most commonly include pain, dysfunction, arthritis, and internal derangement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

In patients with TMD Electromyographic recordings have demonstrated

A

altered muscular contraction,

as well as increased muscular tone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

myofascial pain syndrome (MPS) characterizes by the

A

presence of loci of hypersensitivity within a tender, taut, palpable band of
muscle called a trigger point (TP)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

trigger point

A

TPs are characterized by
referred pain on palpation and elicitation of a local twitch
response (LTR) with application of mechanical pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Trigger points can be classified into

A

active TPs or latent TPs.
Active TPs are described as pain in a motor locus
associated with spontaneous electrical activity, whereas
the more common latent TPs do not cause spontaneous
pain, but can be triggered by factors such as mechanical
stressors, dysfunctional postures, changes in weather, and either excessive immobility or the exaggerated use of muscles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What leads to the formation of a TP circuit?

A

It has been suggested that a positive feedback
cycle involving disproportionate acetylcholine release, sarcomere shortening, and increased concentrations of sensitizing substances leads to the formation of a TP circuit,
which upon connection with other spinal dorsal horn
neuronal pathways, activates latent TPs to become an
active TP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Spine structures functions,

A

protecting the spinal cord, maintaining posture and truncal stability, and acting as a steadying force for movement of the extremities.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Skeletal and ligamentous

structures serve as a

A

protective foundation from which attached muscles provide functional motor control, flexibility, and movement coordination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Weakness in the core muscles
(lumbo-pelvic-hip complex), unbalanced gait mechanics,
or dysfunctional muscular proprioception can
lead to

A

tears, strains, sprains, or spasm within the paraspinal musculature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

True muscle cramps

A

painful involuntary skeletal
muscle contractions associated with electrical activity. EMG studies show fast rates of repetitive firing of motor units in affected muscles. True muscle cramps occur in the absence of fluid or electrolyte imbalance,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

True muscle cramps are

more commonly found in patients with

A

well-developed muscles, in the third trimester of pregnancy, and in metabolic disorders such as cirrhosis and renal disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

causes of muscle cramps include

A

medications, lower motor neuron disease, hypothyroidism, and hereditary
disorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Painful cramps can often be terminated by

A

stretching the cramped muscle.

24
Q

Tricyclic antidepressants (TCAs)

A

amitriptyline, nortriptyline,

desipramine, and imipramine

25
Tricyclic antidepressants (TCAs) Mechanism of Action
provide analgesia independent of their antidepressive effects by multiple mechanisms, which include norepinephrine and serotonin reuptake inhibition in inhibitory descending pathways. Other active mechanisms include blockade of peripheral neural sodium channels, muscarinic and nicotinic acetylcholine receptors, alpha adrenergic receptors, NMDA receptors, substance P release, and to a lesser extent, dopamine receptors
26
TCAs to be effective in | reducing the frequency and intensity of
tension-type headaches (TTHs) and facial pain/TMD.
27
``` Tricyclic antidepressants (TCAs) use is limited secondary to ```
myriad side effects, which include dry mouth, constipation, fluid retention, weight gain, difficulty concentrating, and cardiotoxicity
28
TABLE 18–2
Tricyclic Antidepressants
29
Calcium Channel Antagonists | Pregabalin and gabapentin
an analog of GABA, exert their analgesic effects by acting on the a2-d1 subunit of cellular calcium channels and blocking neurotransmitter release. Their binding to calcium channels results in suppression of abnormal neuronal discharges and an increased threshold for nerve activation
30
most common side effects of gabapentin and pregabalin
include dizziness, sedation, lightheadedness, somnolence, | and weight gain
31
first-line treatment for headache prophylaxis.
gabapentin
32
TABLE 18–3
Calcium Channel Antagonists
33
Gabapentin beneficial
in reducing spasticity in npatients with multiple sclerosis and spinal cord injury and for chronic masticatory myalgia.
34
Usefullness of sodium valproate in Myofascial Pain
an anticonvulsant that acts via a variety of mechanisms including the blockade of T-type calcium and sodium channels, and facilitation of GABA, have shown benefit in TTH and chronic daily headaches
35
Skeletal muscle relaxants
cyclobenzaprine (Flexeril), chlorzoxazone (Paraflex), carisoprodol (Soma), methocarbamol (Robaxin, Robaxisal), tizanidine (Zanaflex), and baclofen (Lioresal)
36
Skeletal muscle relaxants believed to exert their mechanism of action
primarily within the brain and in some cases spinal motor neurons
37
cyclobenzaprine (Flexeril)
Cyclobenzaprine, structurally related to first-generation tricyclic antidepressants, inhibits the reuptake of norepinephrine in the locus coeruleus and inhibits descending serotonergic pathways in the spinal cord. The latter effect may have an inhibitory effect on alpha motor neurons in the spinal cord, resulting in decreased firing and a reduction in mono- and polysynaptic spinal reflexes
38
tizanidine (Zanaflex)
Tizanidine acts as a weak agonist at alpha-2 adrenergic receptors, and enhances presynaptic inhibition at spinal motor neurons
39
Carisoprodol
a precursor of the sedative hypnotic meprobamate, is believed to produce muscle relaxation by blocking interneuronal activity in the descending reticular formation and spinal cord.
40
Baclofen
activates GABA-B receptors in the brain and reduces the release of excitatory neurotransmitters in both the brain and spinal cord. Baclofen also acts by inhibiting the release of substance P in the spinal cord
41
Baclofen Indications
Strong—spasticity of spinal cord origin Moderate—cervical dystonia, upper motor neuron disease, stiff-person syndrome, acute back pain
42
Tizanidine indications
Moderate— spasticity, paravetebral muscle spasm | Weak—TTH
43
Carisoprodol Indications
Moderate—acute musculoskeletal pain, not for spasticity | Weak—TMD
44
Chlorzoxazone (Paraflex, | Parafon, Forte)
Exact mechanism unknown, likely inhibits polysynaptic | reflex pathways in spinal cord (central-acting)
45
Chlorzoxazone (Paraflex, | Parafon, Forte) indications
Moderate—acute musculoskeletal pain, back pain, acute lumbosacral muscle strain
46
Cyclobenzaprine( Flexeril) indications
Strong—cervical and lumbar spinal pain, muscle spasm | Moderate—TMD with myofascial pain
47
Skeletal Muscle Relaxants metabolism and excretion
Liver metabolism | and urine excretion;
48
Skeletal Muscle Relaxants | Adverse Side Effects
Dry mouth, drowsiness, headache, diarrhea, constipation, dizziness, nausea, confusion, lightheadedness,
49
Benzodiazepines Mechanism of Action
enhance presynaptic inhibition in the spinal cord by targeting inhibitory neurotransmitter receptors that are directly activated by GABA. Benzodiazepine receptor binding facilitates GABA A receptor binding, increasing the influx of negatively charged chloride ions across the cell membrane.
50
The increased membrane conductance leads to
hyperpolarization of Ia afferent terminals at neuronal These changes in membrane polarization lead to inhibition of normal neuronal transmission and reduced motor neuron output.synapse
51
Benzodiazepines Common side Effects
include dizziness, somnolence, confusion, memory loss, ataxia, sedation, and physical dependence with sustained use. Psychological effects include paradoxical anxiety, depression, paranoia, and irritability
52
Benzodiazepines
Diazepam (Valium), | Clonazepam (Klonopin), Alprazolam (Xanax), Midazolam (Versed)
53
Benzodiazepines Common | Adverse Side Effects
Drowsiness, dizziness, ataxia, headache, nausea, somnolence, diarrhea, constipation, dry mouth, fatigue, headache, tremor, dysuria, hypotension, tremor, sedation
54
Diazepam Indications
Strong—spasticity of spinal cord origin Moderate—chronic | orofacial muscle pain, tension-type headache Weak—TMD
55
Clonazepam Indications
Moderate—TMD with myofascial | pain, nocturnal muscle spasms
56
Alprazolam Indications
Moderate—TTH